It is well known that electrophysiological heterogeneities arising in the myocardial tissue during acute ischemia, is crucial for unidirectional block (UDB) to ensue. The latter can lead to potentially mortal reentrant arrhythmias, such as ventricular tachycardia and ventricular fibrillation. In fact, differences in action potential duration (APD), refractory period (RP) and conduction velocity (CV) are the main responsible for the generation and maintenance of reentrant episodes, being the RP an aspect of great interest. Most studies suggest that dispersion of PR plays a proarrhythmic role. However, some investigations do not support this hypothesis. In the last decades, the huge advances in computational resources have made possible the simulation of cellular electrical activity with a high level of electrophysiological detail and realism. This investigation technique can give insight about ionic processes impossible to extract experimentally.
This work is aimed to unravel the underlying mechanisms of conduction block that result in reentrant activity during acute myocardial ischemia. For this purpose, the electrical activity of an epicardial 2D tissue has been simulated using a modified version of the Luo-Rudy dynamic AP model (LRd00) and a realistic model of regional ischemia. Furthermore, from the point of view of computational requirements, an optimal formulation of the safety factor of conduction (SF) has been proposed, which ables the study of the relevant source-sink relationship in bidimensional tissues. 
Our results demonstrate that during myocardial ischemia phase Ia, the vulnerable window of a bidimensional tissue, indicator for vulnerability to reentry, has an asymmetric unimodal distribution, peaking at minute eight after coronary occlusion. We obtained arrhythmic episodes as stable figure of eight reentries. Simultaneously, as ischemia progresses, the restitution curve flattens, the SF decreases and the heterogeneity of refractoriness grows. Therefore, a lack of correlation between dispersion of refractoriness and vulnerability to reentry is observed. In fact, in approximately 50% of the obtained reentries, UDB takes place in cells completely recovered from refractoriness but with an unbalanced source-sink relationship.  
Regarding the involved ionic mechanisms, hyperkalemia is crucial in reentry generation and moderated acidosis and hypoxia play a synergic role in this phenomenon.
In conclusion, the UDB leading to reentry results from the mismatch of the source-sink relationship. Additionally, this property strongly depends on the axial currents resulting from the membrane excitability, refractoriness and their inhomogeneity, among other factors.